Inhaled nanoparticles – like those released from vehicle exhausts – can work their way through the lungs and into the bloodstream, potentially raising the risk of heart attack and stroke, according to new research part-funded by the British Heart Foundation. The findings, published today in the journal ACS Nano, build on previous studies that have found tiny particles in air pollution are associated with an increased risk of cardiovascular disease, although the cause remains unproven. However, this research shows for the first time that inhaled nanoparticles can gain access to the blood in healthy individuals and people at risk of stroke. Most worryingly, these nanoparticles tend to build-up in diseased blood vessels where they could worsen coronary heart disease – the cause of a heart attack.

It is not currently possible to measure environmental nanoparticles in the blood. So, researchers from the University of Edinburgh, and the National Institute for Public Healthand the Environment in the Netherlands, used a variety of specialist techniques to track the fate of harmless gold nanoparticles breathed in by volunteers. They were able to show that these nanoparticles can migrate from the lungs and into the bloodstream within 24 hours after exposure and were still detectable in the bloodthree months later. By looking at surgically removed plaques from people at high risk of stroke they were also able to find that the nanoparticles accumulated in the fatty plaques that grow inside blood vessels and cause heart attacks and strokes. Cardiovascular disease (CVD) – the main forms of which are coronary heart disease and stroke – accounts for 80% of all premature deaths from air pollution.

“It is striking that particles in the air we breathe can get into our blood where they can be carried to different organs of the body. Only a very small proportion of inhaled particles will do this, however, if reactive particles like those in air pollution then reach susceptible areas of the body then even this small number of particles might have serious consequences,” said Dr Mark Miller, Senior Research Fellow at the University of Edinburgh who led the study.

As men and women grow older, their chances for coronary heart disease also increase. Atherosclerosis is a condition in which plaque builds up inside the arteries, which can lead to serious problems, including heart attacks, strokes or even death. Now, researchers at the University of Missouri (MU) have found that Insulin-like Growth Factor-1 (IGF-1), a protein that is naturally found in high levels among adolescents, can help prevent arteries from clogging. They say that increasing atherosclerosis patients’ levels of the protein could reduce the amount of plaque buildup in their arteries, lowering their risk of heart disease.

“The body already works to remove plaque from arteries through certain types of white blood cells called macrophages,” said Yusuke Higashi, PhD, assistant research professor in the Division of Cardiovascular Medicine at the MU School of Medicine and lead author of the study. “However, as we age, macrophages are not able to remove plaque from the arteries as easily. Our findings suggest that increasing IGF-1 in macrophages could be the basis for new approaches to reduce clogged arteries and promote plaque stability in aging populations.”

In a previous study, Higashi and Patrice Delafontaine, MD, the Hugh E. and Sarah D. Stephenson Dean of the MU School of Medicine, examined the arteries of mice fed a high-fat diet for eight weeks. IGF-1 was administered to one group of mice. Researchers found that the arteries of mice with higher levels of IGF-1 had significantly less plaque than mice that did not receive the protein. Since the macrophage is a key player in the development of atherosclerosis, the researchers decided to investigate potential anti-atherosclerosis effects of IGF-1 in macrophages. The team also found that the lack of IGF-1 action in macrophages changed the composition of the plaque, weakening its strength and making it more likely to rupture and cause a heart attack.

A particularly high number of people suffer from arteriosclerosis—with fatal consequences: Deposits in the arteries lead to strokes and heart attacks. A team of researchers under the leadership of the University of Bonn has now developed a method for guidingreplacement cells to diseased vascular segments using nanoparticles. The scientists demonstrated in mice that the fresh cells actually exert their curative effect in these segments.

In arterial calcification (arteriosclerosis), pathological deposits form in the arteries and this leads to vascular stenosis. Strokes and heart attacks are a frequent outcome due to the resultant insufficient blood flow. Endothelial cells which line the blood vessels play an important role here. Damage to the endothelial cells is generally the insidious onset of arteriosclerosis.

The scientists introduced tiny nanoparticles with an iron core. “The iron changes the properties of the endothelial cells: They become magnetic,” explains Dr. Sarah Rieck from the Institute of Physiology I of the University of Bonn. The nanoparticles ensure that the endothelial cells equipped with the ‘turbo‘ gene can be delivered to the desired site in the blood vessel using a magnet where they exert their curative effect.

The researchers tested this combination method in mice whose carotid artery endothelial cells were injured. They injected the replacement cells into the artery and were able to position them at the correct site using the magnet. “After half an hour, the endothelial cells adhered so securely to the vascular wall that they could no longer be flushed away by the bloodstream,” says Jun.-Prof. Wenzel. The scientists then removed the magnets and tested whether the fresh cells had fully regained their function. As desired, the new endothelial cells produced nitric oxide and thus expanded the vessel, as is usual in the case of healthy arteries. “The mouse woke up from the anesthesia and ate and drank normally,” reported the physiologist.

In what may be a major leap forward in the quest for new treatments of the most common form of cardiovascular disease, scientists at Johns Hopkins report they have found a way to halt and reverse the progression of atherosclerosis in rodents by loading microscopic nanoparticles with a chemical that restores the animals’ ability to properly handle cholesterol.

Cholesterol is a fatty substance that clogs, stiffens and narrows the blood vessels, greatly diminishing their ability to deliver blood to the heart muscle and the brain. The condition, known as atherosclerotic vessel disease, is the leading cause of heart attacks and strokes that claim some 2.6 million lives a year worldwide, according to the World Health Organization.

A report on the work, published online in the journal Biomaterials, builds on recent research by the same team that previously identified a fat-and-sugar molecule called GSL as the chief culprit behind a range of biological glitches that affect the body’s ability to properly use, transport and purge itself of vessel-clogging cholesterol.

That earlier study showed that animals feasting on high-fat foods remained free of heart disease if pretreated with a man-made compound, D-PDMP, which works by blocking the synthesis of the mischievous GSL. But the body‘s natural tendency to rapidly break down and clear out D-PDMP was a major hurdle in efforts to test its therapeutic potential in larger animals and humans. The newly published report reveals the scientists have cleared that hurdle by encapsulating D-PDMP into tiny molecules, which are absorbed faster and linger in the body much longer. In this case, the researchers say, their experiments show that when encapsulated that way, D-PDMP’s potency rose ten-fold in animals fed with it. Most strikingly, the team reports, the nano version of the compound was potent enough to halt the progression of atherosclerosis. As well, the nano-packaged drug improved physiologic outcomes among animals with heart muscle thickening and pumping dysfunction, the hallmarks of advanced disease.

“Our experiments illustrate clearly that while content is important, packaging can make or break a drug,” says lead investigator Subroto Chatterjee, Ph.D., a professor of medicine and pediatrics at the Johns Hopkins University School of Medicine and a metabolism expert at its Heart and Vascular Institute. “In our study, the right packaging vastly improved the drug’s performance and its ability not merely to prevent disease but to mitigate some of its worst manifestations.”

NYU Polytechnic School of Engineering professors have been collaborating with researchers from Peking University on a new test strip that is demonstrating great potential for the early detection of certain heart attacks.

Kurt H. Becker, a professor in the Department of Applied Physics, and WeiDong Zhu, a research associate professor in the Department of Mechanical Engineering, are helping develop a new colloidal gold test strip for cardiac troponin I (cTn-I) detection. The new strip uses microplasma-generated gold nanoparticles (AuNPs) and shows much higher detection sensitivity than conventional test strips. The new cTn-I test is based on the specific immune-chemical reactions between antigen and antibody on immunochromatographic test strips using AuNPs.
Compared to AuNPs produced by traditional chemical methods, the surfaces of the gold nanoparticles generated by the microplasma-induced liquid chemical process attract more antibodies, which results in significantly higher detection sensitivity.